acts as a pathobiont promoting the biofilm virulence and cariogenicity of in adult severe caries.

Adult severe caries (ASC) brings severe oral dysfunction and treatment difficulties to patients, and yet no clear pathogenic mechanism for it has been found. This study is focused on the composition of dental plaque microbiome profiles in order to identify disease-relevant species and to investigate into their interactions with the . Samples of dental plaque were collected for metagenomic analysis. The acidification, aciduricity, oxidative stress tolerance, and (glucosyltransferase) gene expression of cocultured with which was identified as ASC-related dominant bacterium. The biofilm formation and extracellular exopolysaccharide (EPS) synthesis of dual-strain were analyzed with scanning electron microscopy (SEM), crystal violet (CV) staining, live/dead bacterial staining, and confocal laser scanning microscopy (CLSM). Furthermore, rodent model experiments were performed to validate the cariogenicity of the dual-species biofilm. The most significantly abundant taxon found associated with ASC was . experiments found that can effectively promote mature biofilm formation with enhanced acid resistance, hydrogen peroxide detoxicity, and biofilm virulence. Rodent model experiments revealed that was incapable of causing disease on its own, but it significantly heightened the biofilm virulence of when being co-infected and augmented the progression, quantity, and severity of dental caries. Our findings demonstrated that may act as a synergistic pathobiont to modulate the metabolic activity, spatial structure, and pathogenicity of biofilms of in the context of ASC.IMPORTANCEAdult severe caries (ASC), as a special type of acute caries, is rarely reported and its worthiness of further study is still in dispute. Yet studies on the etiology of severe caries in adults have not found a clear pathogenic mechanism for it. Knowledge of the oral microbiota is important for the treatment of dental caries. We discovered that the interaction between and augments the severity of dental caries , suggesting may act as a synergistic pathobiont exacerbating biofilm virulence of in ASC. Our findings may improve the understanding of ASC pathogenesis and are likely to provide a basis for planning appropriate therapeutic strategies.